For the past year, we have attempted to characterize various facets of cognitive abnormalities in schizophrenia. Kolb had been especially interested in attempting to delineate the cognitive components of subprocesses involved in various paradigms. 1. We have continued our work examining the relationship between thought disorder and abnormalities in semantic memory. We have assessed patients on semantic memory measures while receiving neuroleptic medications and while receiving placebo. In addition, we have examined semantic organization by using a "triadic" pair comparison task in order to assess the stability of semantic organization over time in patients and in normals. Furthermore, we have developed a visual semantic test based on notions of semantic boundaries between objects. 2. We have examined working memory in two paradigms. First, we have continued our work on understanding the "n-bac" task and have assessed large numbers of normal individuals and found a linear increase in difficulties that was consistent with our predictions about specific task manipulations (e.g., the addition of catch trials, increasing delays). Second, we have looked at the Brown-Peterson task and systematically manipulated delay, memory load and interference. We found that capacity limitations and failures in central executive rather than slave system performance were associated most strongly with schizophrenia. Delay did not have a differential effect on patients. 3. We have devised a series of tests to better understand the cognitive components of the CPT. We will examine working memory, stimulus response mapping, and response preparation as alternatives in more fundamental processes associated with CPT performance. 4. In order to assess specificity of cognitive impairment in schizophrenia, we examined patients with traumatic brain injury. We found marked differences between them and patients with schizophrenia. Patients with schizophrenia performed significantly worse on a wide variety of tasks. It should be noted that the patients with traumatic brain injury had significant degrees of posttraumatic amnesia (i.e., >2 weeks). We suggest that the degree of impairment in schizophrenia is quite severe. 5. We have commenced a large study in which we will use cognitive variables as phenotypic markers and attempt to link these to allelic abnormalities in schizophrenia in order to better understand genetic susceptibility to this disorder. In particular, it is our hypothesis that neurocognitive measures may be better phenotypic markers than symptom based diagnosis.